Rickets (scientific nomenclature: rachitis; from Greek ῥαχίτης rhakhítēs, meaning "in or of the spine" which was chosen as a back-formation, see Etymology) is a condition that results in weak or soft bones in children and may have either dietary-deficiency or genetic causes. Symptoms include bowed legs, stunted growth, bone pain, large forehead, and trouble sleeping. Complications may include bone deformities, bone pseudofractures and fractures, muscle spasms, or an abnormally curved spine. The analogous condition in adults is osteomalacia. One can characterise a child who appears to suffer from rickets as rachitic. The most common cause of rickets is a vitamin-D deficiency, although hereditary genetic forms also exist. The condition can result from eating a diet without enough vitamin D, dark skin, too little sun exposure, exclusive breastfeeding without vitamin D supplementation, celiac disease, and certain genetic conditions. Other factors may include not enough calcium or phosphorus. The underlying mechanism involves insufficient calcification of the growth plate. Diagnosis is generally based on blood tests finding a low calcium, low phosphorus, and a high alkaline phosphatase together with X-rays. Prevention for exclusively breastfed babies is vitamin D supplements. Otherwise, treatment depends on the underlying cause. If due to a lack of vitamin D, treatment is usually with vitamin D and calcium. This generally results in improvements within a few weeks. Bone deformities may also improve over time. Occasionally, surgery may be performed to correct bone deformities. Genetic forms of the disease typically require specialized treatment. Rickets occurs relatively commonly in the Middle East, Africa, and Asia. It is generally uncommon in the United States and Europe, except among certain minority groups, but rates have been increasing among some populations. It begins in childhood, typically between the ages of 3 and 18 months of age. Rates of disease are equal in males and females. Cases of what is believed to have been rickets have been described since the 1st century AD, and the condition was widespread in the Roman Empire. The disease occurred commonly into the 20th century. Early treatments included the use of cod liver oil.
Signs and symptoms Signs and symptoms of dietary deficiency rickets can include bone tenderness, and a susceptibility for bone fractures, particularly greenstick fractures. Early skeletal deformities can arise in infants such as soft, thinned skull bones – a condition known as craniotabes, which is the first sign of rickets; skull bossing may be present and a delayed closure of the fontanelles. Young children may have bowed legs and thickened ankles and wrists; older children may have knock knees. Spinal curvatures of kyphoscoliosis or lumbar lordosis may be present. The pelvic bones may be deformed. A condition known as rachitic rosary can result from the thickening caused by nodules forming on the costochondral joints. This appears as a visible bump in the middle of each rib in a line on each side of the body. This somewhat resembles a rosary, giving rise to its name. The deformity of a pigeon chest may result in the presence of Harrison's groove. Hypocalcemia, a low level of calcium in the blood, can result in tetany – uncontrolled muscle spasms. Dental problems can also arise. An X-ray or radiograph of an advanced patient with rickets tends to present in a classic way: the bowed legs (outward curve of long bones of the legs) and a deformed chest. Changes in the skull also occur, causing a distinctive "square-headed" appearance known as "caput quadratum". These deformities persist into adult life if not treated. Long-term consequences include permanent curvatures or disfiguration of the long bones, and a curved back.
Cause Maternal deficiencies may be the cause of overt bone disease from before birth and impairment of bone quality after birth. The primary cause of congenital rickets is vitamin D deficiency in the mother's blood. Vitamin D ensures that serum phosphate and calcium levels are sufficient to facilitate the mineralization of bone. Congenital rickets may also be caused by other maternal diseases, including severe osteomalacia, untreated celiac disease, malabsorption, pre-eclampsia, and premature birth. Rickets in children is similar to osteomalacia in adults, and differs from osteoporosis, where there is increased porosity of bone leading to brittleness.. Prenatal care includes checking vitamin levels and ensuring that any deficiencies are supplemented. Exclusively breast-fed infants may require rickets prevention by vitamin D supplementation or increased exposure to sunlight. In sunny countries such as Nigeria, South Africa, and Bangladesh, there is sufficient endogenous vitamin D due to exposure to the sun. However, the disease occurs among older toddlers and children in these countries, which in these circumstances is attributed to low dietary calcium intakes due to a mainly cereal-based diet. Those at higher risk for developing rickets include:
Breast-fed infants whose mothers are not exposed to sunlight Breast-fed infants who are not exposed to sunlight Breast-fed babies who are exposed to little sunlight Adolescents, in particular when undergoing the pubertal growth spurt Any child whose diet does not contain enough vitamin D or calcium Diseases causing soft bones in infants, like hypophosphatasia or hypophosphatemia, can also lead to rickets. Strontium is allied with calcium uptake into bones; at excessive dietary levels, strontium has a rachitogenic (rickets-producing) action.
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